The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Inhibition of ferroptosis attenuates tissue damage and improves long‐term outcomes after traumatic brain injury in mice
Open accessAbstract
Summary: Aims: Ferroptosis, a new form of iron‐dependent programmed cell death, has been shown to be involved in a range of diseases. However, the role of ferroptosis in traumatic brain injury (TBI) has yet to be elucidated. We aimed to investigate whether ferroptosis is induced after TBI and whether the inhibition of ferroptosis would protect against traumatic brain injury in a controlled cortical impact injury (CCI) mouse model. Methods: After establishing the TBI model in mice, we determined the biochemical and morphological changes associated with ferroptosis, including iron accumulation with Perl's staining, neuronal cell death with Fluoro‐Jade B (FJB) staining, iron metabolism dysfunction with Western blotting, reactive oxygen species (ROS) accumulation with malondialdehyde (MDA) assays, and shrunken mitochondria with transmission electron microscopy. Furthermore, a specific inhibitor of ferroptosis, ferrostatin‐1(fer‐1), was administrated by cerebral ventricular injection after CCI. We used cresyl violet (CV) staining to assess lesion volume, along with the Morris water maze and beam walk test to evaluate long‐term outcomes. Results: TBI was followed by iron accumulation, dysfunctional iron metabolism, the upregulation of ferroptosis‐related genes, reduced glutathione peroxidase (GP x) activity, and the accumulation of lipid‐reactive oxygen species (ROS). Three days (d) after TBI, transmission electron microscopy (TEM) confirmed that the mitochondria had shrunk a typical characteristic of ferroptosis. Importantly, the administration of Fer‐1 by cerebral ventricular injection significantly reduced iron deposition and neuronal degeneration while attenuating injury lesions and improving long‐term motor and cognitive function. Conclusion: This study demonstrated an effective method with which to treat TBI by targeting ferroptosis.
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Ferroptosis: past, present and future
Li, J., Cao, F., Yin, H.-L., Huang, Z.-J., Lin, Z.-T., Mao, N., Sun, B., & Wang, G. (2020) · Cell Death & Disease · doi:10.1038/s41419-020-2298-2 · Cited by 4,171
Iron Homeostasis and Ferroptosis in Human Diseases: Mechanisms and Therapeutic Prospects
Ru, Q., Li, Y., Chen, L., Wu, Y., Min, J., & Wang, F. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01969-z · Cited by 724
Redox lipid reprogramming commands susceptibility of macrophages and microglia to ferroptotic death
Kapralov, A. A., Yang, Q., Dar, H. H., Tyurina, Y. Y., Anthonymuthu, T. S., Kim, R., St. Croix, C. M., Mikulska-Ruminska, K., Liu, B., Shrivastava, I. H., et al. (2020) · Nature Chemical Biology · doi:10.1038/s41589-019-0462-8 · Cited by 650
Bai, T., Li, M., Liu, Y., Qiao, Z., & Wang, Z. (2020) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2020.07.026 · Cited by 532
The application of Ferroptosis in diseases
Qiu, Y., Cao, Y., Cao, W., Jia, Y., & Lu, N. (2020) · Pharmacological Research · doi:10.1016/j.phrs.2020.104919 · Cited by 415
Metadata
- Authors
- Xie, B., Wang, Y., Lin, Y., Mao, Q., Feng, J., Gao, G., & Jiang, J.
- Venue
- CNS Neuroscience & Therapeutics
- Publisher
- Wiley
- Published
- 2018-09-28
- Volume
- 25
- Issue
- 4
- Pages
- 465-475
- ISSN
- 1755-5930 (ISSN-L)
- 1755-5949
- OpenAlex
- W2893339118
- Cited by
- 389
- References
- 43
- FWCI
- 11.12
- Type
- journal article
- Language
- en
- Open access
- green
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- Xie, B., Wang, Y., Lin, Y., Mao, Q., Feng, J., Gao, G., & Jiang, J. (2019). Inhibition of ferroptosis attenuates tissue damage and improves long‐term outcomes after traumatic brain injury in mice. CNS Neuroscience & Therapeutics. https://doi.org/10.1111/cns.13069
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